GLUT5-KHK axis-mediated fructose metabolism drives proliferation and chemotherapy resistance of colorectal cancer

Shen, Zhiyong; Li, Zhenkang; Liu, Yuechen; Li, Yongsheng; Feng, Xiaochuang; Zhan, Yizhi; Lin, Mingdao; Fang, Chuanfa; Fang, Yuan; Deng, Haijun

doi:10.1016/j.canlet.2022.215617

Cited by 20 publications

(16 citation statements)

References 36 publications

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“…Unfortunately, while these drugs induce tumor cell apoptosis, they also force tumor cells to undergo adaptive changes such as mutations of antiapoptotic genes or the generation of drug resistance genes. Although numerous studies on chemotherapy resistance have been conducted in the past 20 years, there seems to be not much substantial progress ( 27 , 28 ). The currently accepted way to circumvent or delay the occurrence of chemotherapy resistance is to combine chemotherapy with other drugs, such as immune checkpoint inhibitors or anti-EGFR targeted drugs.…”

Section: Discussionmentioning

confidence: 99%

Publication trends and hotspots of drug resistance in colorectal cancer during 2002-2021: A bibliometric and visualized analysis

Zhao

Jiao

et al. 2022

Front. Oncol.

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BackgroundChemotherapy, radiotherapy, targeted therapy and immunotherapy have demonstrated expected clinical efficacy, while drug resistance remains the predominant limiting factor to therapeutic failure in patients with colorectal cancer (CRC). Although there have been numerous basic and clinical studies on CRC resistance in recent years, few publications utilized the bibliometric method to evaluate this field. The objective of current study was to provide a comprehensive analysis of the current state and changing trends of drug resistance in CRC over the past 20 years.MethodsThe Web of Science Core Collection (WOSCC) was utilized to extracted all studies regarding drug resistance in CRC during 2002-2021. CiteSpace and online platform of bibliometrics were used to evaluate the contributions of various countries/regions, institutions, authors and journals in this field. Moreover, the recent research hotspots and promising future trends were identified through keywords analysis by CiteSpace and VOSviewer.Results1451 related publications from 2002 to 2021 in total were identified and collected. The number of global publications in this field has increased annually. China and the USA occupied the top two places with respect to the number of publications, contributing more than 60% of global publications. Sun Yat-sen University and Oncotarget were the institution and journal which published the most papers, respectively. Bardelli A from Italy was the most prolific writer and had the highest H-index. Keywords burst analysis identified that “Growth factor receptor”, “induced apoptosis” and “panitumumab” were the ones with higher burst strength in the early stage of this field. Analysis of keyword emergence time showed that “oxaliplatin resistance”, “MicroRNA” and “epithelial mesenchymal transition (EMT)” were the keywords with later average appearing year (AAY).ConclusionsThe number of publications and research interest on drug resistance in CRC have been increasing annually. The USA and China were the main driver and professor Bardelli A was the most outstanding researcher in this field. Previous studies have mainly concentrated on growth factor receptor and induced apoptosis. Oxaliplatin resistance, microRNA and EMT as recently appeared frontiers of research that should be closely tracked in the future.

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Section: Discussionmentioning

confidence: 99%

Publication trends and hotspots of drug resistance in colorectal cancer during 2002-2021: A bibliometric and visualized analysis

Zhao

Jiao

et al. 2022

Front. Oncol.

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“…have reported that multiple human CRC cell lines (ex. HCT116 and HT29) upregulated GLUT5 expression in response to glucose depletion, which led to the increased uptake of fructose and its metabolism to fuel central carbon metabolism ( 28 ). Furthermore, the study also found that fructose-induced levels of GLUT5 proteins could bind to KHK and block its lysosomal degradation, further sustaining its metabolism of fructose ( 28 ).…”

Section: Colon-rectal Cancer and Intestinal Cancermentioning

confidence: 99%

Fructose-induced metabolic reprogramming of cancer cells

Ting

2024

Front. Immunol.

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Excess dietary fructose consumption has been long proposed as a culprit for the world-wide increase of incidence in metabolic disorders and cancer within the past decades. Understanding that cancer cells can gradually accumulate metabolic mutations in the tumor microenvironment, where glucose is often depleted, this raises the possibility that fructose can be utilized by cancer cells as an alternative source of carbon. Indeed, recent research has increasingly identified various mechanisms that show how cancer cells can metabolize fructose to support their proliferating and migrating needs. In light of this growing interest, this review will summarize the recent advances in understanding how fructose can metabolically reprogram different types of cancer cells, as well as how these metabolic adaptations can positively support cancer cells development and malignancy.

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“…[4] Some studies have reported some resistance mechanisms, such as the action of dual specificity protein phosphatases (DUSPs) as an enhancer of cell death resistance. [23] The role of the GLUT5 transporter in inhibiting cell death, increased cell proliferation, colony formation, and increased ability to fight chemotherapeutic drugs through fructose metabolism mediated by this transporter in the absence of glucose [24] and P-glycoprotein that can act as a drug efflux pump influencing chemoresistance. [25] The anticancer treatments currently used lead to side effects in patients.…”

Section: Repositioning Antimicrobial Peptides For Cancer Treatmentmentioning

confidence: 99%

Recalculating the Route: Repositioning Antimicrobial Peptides for Cancer Treatment

de Almeida Gomes,

da Lima,

da Silva Brito

et al. 2023

Chemistry & Biodiversity

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Resistance to antimicrobial drugs has been considered a public health problem. Likewise, the increasing resistance of cancer cells to drugs currently used in therapy has also become a problem. Therefore, the research and development of synthetic peptides bring a new perspective on the emergence of new drugs for treating this resistance since bioinformatics provides a means to optimize these molecules and save time and costs in research. Peptides have several mechanisms of action, such as forming pores on the cell membrane and inhibiting protein synthesis. Some studies report the use of antimicrobial peptides with the potential for action against cancer cells, suggesting a repositioning of antimicrobial peptides to fight back cancer resistance. There is an alteration in the microenvironment, making its net charge negative for the survival and growth of cancer cells. The changes in glycoproteins favor the membrane to have a more negative charge, favoring the interaction between the cells and the peptide, thus making possible the repositioning of these antimicrobial peptides against cancer. Here, we will discuss the mechanism of action, targets and effects of peptides, comparison between microbial and cancer cells, and proteomic changes caused by the interaction of peptides and cells.

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GLUT5-KHK axis-mediated fructose metabolism drives proliferation and chemotherapy resistance of colorectal cancer

Cited by 20 publications

References 36 publications

Publication trends and hotspots of drug resistance in colorectal cancer during 2002-2021: A bibliometric and visualized analysis

Publication trends and hotspots of drug resistance in colorectal cancer during 2002-2021: A bibliometric and visualized analysis

Fructose-induced metabolic reprogramming of cancer cells

Recalculating the Route: Repositioning Antimicrobial Peptides for Cancer Treatment

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